Activity of peripheral sympathetic efferent nerves in experimental subarachnoid haemorrhage. Part II: Observations during the "early vasospasm" period.

The efferent activity of the vertebral, cardiac and renal sympathetic nerves was recorded during the so-called "early vasospasm" period, 25-30 minutes after experimentally induced subarachnoid haemorrhage. Experiments were performed on 51 cats with methods described in Part I of our publication. The animals were held either in a sphynx-like position (Pos. I), or in head-down position (Pos. II), when the level of the cisterna magna was 2-3 cm below the level of the spinal cord, facilitating the injected blood to flow in to, and remain at the base of the brain. According to our results during the "early vasospasm" period, we could not observe such changes in the sympathetic efferent activity, which could be specific for this period. With the gradual decrease in the intracranial pressure, the sympathetic overactivity ceased, and in most cases the level of activity was similar to that of the preinjection period. Our results also indicate that because of the remarkable variability of the activity of the renal sympathetic nerve during the intracranial pressure elevation, recording the activity of one sympathetic nerve only may give misleading results concerning the activity of the whole sympathetic system.

Activity of peripheral sympathetic efferent nerves in experimental subarachnoid haemorrhage. Part I: Observations at the time of intracranial hypertension.

The origin and pathomechanism of vegetative disturbances in patients suffering from subarachnoid haemorrhage are not completely clarified. Since some of these alterations in vegetative functions may well be attributed to acute changes in sympathetic activity, we initiated a study to investigate this modality in experimentally induced subarachnoid haemorrhage. Experiments were performed on 51 cats, anaesthetized with alpha-chloralose and urethane, immobilized and artificially ventilated. Compound electrical discharges of the left vertebral, cardiac and renal sympathetic nerves, ECG, EEG, end-tidal CO2, systemic arterial blood pressure and intracranial pressure were recorded on a polygraph. Subarachnoid haemorrhage was simulated by the injection of 1-5 ml of fresh, autologous blood into the cisterna magna. Mock cerebrospinal fluid was also injected as a control. Our results showed that in induced subarachnoid haemorrhage, not the blood itself but the intracranial pressure elevation might be responsible for the strong increase in sympathetic efferent activity. With the direct recording of the electrical activity of the three sympathetic nerves, we were able to verify the sympathetic overactivity underlying the cardiovascular disturbances during intracranial pressure elevation. Regarding the mechanism of the overactivity, most probably not the ischaemia or hypoxia, but the mechanical distortion of the medulla could be the adequate stimulus of the sympathetic overactivity and the Cushing response during intracranial pressure elevation.